Glycan cross-feeding supports mutualism between Fusobacterium and the vaginal microbiota.

Women with bacterial vaginosis (BV), an imbalance of the vaginal microbiome, are more likely to be colonized by potential pathogens such asFusobacterium nucleatum, a bacterium linked with intrauterine infection and preterm birth. However, the conditions and mechanisms supporting pathogen colonization during vaginal dysbiosis remain obscure. We demonstrate that sialidase activity, a diagnostic feature of BV, promotedF.nucleatumforaging and growth on mammalian sialoglycans, a nutrient resource that was otherwise inaccessible because of the lack of endogenousF.nucleatumsialidase. In mice with sialidase-producing vaginal microbiotas, mutantF.nucleatumunable to consume sialic acids was impaired in vaginal colonization. These experiments in mice also led to the discovery thatF.nucleatummay also "give back" to the community by reinforcing sialidase activity, a biochemical feature of human dysbiosis. Using human vaginal bacterial communities, we show thatF.nucleatumsupported robust outgrowth ofGardnerella vaginalis, a major sialidase producer and one of the most abundant organisms in BV. These results illustrate that mutually beneficial relationships between vaginal bacteria support pathogen colonization and may help maintain features of dysbiosis. These findings challenge the simplistic dogma that the mere absence of "healthy" lactobacilli is the sole mechanism that creates a permissive environment for pathogens during vaginal dysbiosis. Given the ubiquity ofF.nucleatumin the human mouth, these studies also suggest a possible mechanism underlying links between vaginal dysbiosis and oral sex.